Uterine Inversion and Uterine Rupture

Uterine Inversion and Uterine Rupture

Amanda Sue Shorette


Uterine inversion and uterine rupture are rare but life-threatening obstetric complications. There is a paucity of available data regarding the epidemiology, risk factors, and pathogenesis of these conditions. Both conditions, however, warrant special attention given the potential for severe maternal morbidity and mortality. Prompt recognition and management is essential, as any delay in diagnosis or inappropriate treatment can lead to severe hemorrhage, shock, and even maternal death.


Overview and Background

Uterine inversion is an obstetric emergency that occurs when the uterine fundus collapses into the endometrial cavity. It is often associated with marked maternal hemorrhage and subsequent cardiovascular collapse.1 Epidemiologic data on uterine inversion are limited, consisting of case reports, small center case series, and a few nationwide studies.2,3,4 As a result, the incidence is difficult to define, with estimates ranging widely from 1 in 1,200 to 1 in 57,000, with a range of 1 in 20,000 most commonly reported.1,2,4,5,6,7 Uterine inversion occurs most often in the third stage of labor during vaginal delivery, but has also been described with cesarean delivery.1,2,4,5,6 Approximately 5% of cases are spontaneous non-puerperal uterine inversions, which are almost always associated with a uterine tumor such as leiomyoma, teratoma, or sarcoma.3,4


When uterine inversion is recognized and treated immediately, overall mortality is quite low. Mortality rates range from 15% to 41% in older series, but recent maternal mortality rates in developed countries is lacking. Unfortunately, in low resource countries, maternal deaths from uterine inversion are still described.2,3 However, many cases are associated with immediate life-threatening hemorrhage and shock, with nearly half requiring blood replacement.3,5,8 One series of 2,427 cases of puerperal uterine inversion in the United States between 2004 and 2013 showed that postpartum hemorrhage occurred in 37.7% of cases; there was need for blood transfusion in 22.4%; laparotomy in 6%; and hysterectomy in 2.8%. This series also described maternal hypotension and shock
in 3.4% of cases with one maternal death.2 Another study done in the Netherlands cited a much higher incidence of morbidity, with 60% of patients requiring blood products for resuscitation and profound anemia (hemoglobin <5), as well as 47% identified as having shock.3

The risk of recurrence in future pregnancies is not well defined. The American College of Obstetrics and Gynecology (ACOG) reports that uterine inversion in a prior pregnancy increases risk to 1 per 26 subsequent deliveries.1 One series of 40 cases showed no recurrences in 26 subsequent deliveries.4 Overall, the incidence of recurrent inversions appears to be low.

Pathophysiology and Risk Factors

The pathogenesis of uterine inversion is incompletely understood, but a number of contributing factors have been identified. Excessive cord traction before placental separation and fundal pressure (Credé maneuver) during the third stage of labor are the most common causes of inversion cited.2,4,5 However, a direct causal relationship has not been established. It is likely that many factors are at play, given reported spontaneous inversions without either of these conditions present in addition to the common performance of both cord traction and Credé maneuver uncomplicated by uterine inversion.4,7 Placental abnormalities, including fundal implantation and abnormally adhered placentation such as accreta syndromes, have also been identified as risk factors.4,5,6,7,8 Additional risk factors include atonic uterus, fetal macrosomia, rapid labor and delivery, prolonged labor and delivery, short umbilical cord, use of uterine relaxants, nulliparity, uterine anomalies or tumors, and retained placenta.3,4,7 Risk factors are identified, however, in less than 50% of cases.2 In addition, a study demonstrates that despite knowing these risk factors, the vast majority of women identified as having uterine inversion were deemed to have been low risk prior to labor and delivery.3


Uterine inversion is described based on the extent of inversion as well as timing.4,6,7,8 The extent of uterine protrusion, which often correlates with severity, is classified into four degrees (Figure 28.1). First degree or incomplete uterine inversion occurs when the fundus prolapses into the endometrial cavity. With second degree or complete inversion, the fundus protrudes through the cervical os. Third-degree inversion (uterine prolapse) describes protrusion of the fundus to or beyond the introitus. Both the uterus and vagina are inverted with fourth-degree (total uterine and vaginal) inversion, which can be catastrophic with severe bleeding. Uterine inversion is further characterized as being acute (onset within 24 hours of delivery), subacute (24 hours to 4 weeks postpartum), or chronic (>1 month postpartum). The vast majority, 83% of cases, are acute, with 14% presenting as chronic and 3% as subacute.4

Clinical Features


Imaging is rarely needed as the diagnosis is made clinically in the setting of vaginal bleeding, pain, visualization or palpation of an inverted uterus, and absence of the uterine fundus on abdominal examination. However, ultrasound and magnetic resonance imaging (MRI) can be utilized when the diagnosis is uncertain and the patient is hemodynamically stable.4,9 Imaging should never delay care in the patient with significant bleeding and shock. Ultrasound has the capability of being used
at the patient’s bedside and therefore should be the imaging modality of choice in the emergent setting. Ultrasound will show an abnormal uterine fundal contour with a homogenous globular mass (inverted fundus) within the uterus or vagina.4,9,10,11


Initial Presentation

Treatment guidelines for the management of uterine inversion are based on the best available evidence from case reports, small retrospective case series describing effective treatment options, and expert opinion.4 The following primary interventions should occur immediately and simultaneously, for any delay in management can result in significant maternal morbidity and mortality (Figure 28.2).4,5,6,7,8

  • Discontinue uterotonic drugs. Immediately discontinue uterotonic agents such as oxytocin, because uterine relaxation is needed for uterine replacement. Over time the lower uterine segment and cervix will begin to contract, resulting in a cervical ring making manual replacement of the uterus even more difficult. Use of uterotonic agents will only exacerbate this process.1,4,5,6,7,8

  • Call for immediate assistance. Call for additional help from the emergent obstetric team. Mobilize anesthesiology and operating room staff early on, as the patient may require operative management if manual replacement is unsuccessful.

  • Establish adequate intravenous (IV) and initiate aggressive fluid resuscitation. Two large-bore IVs should be placed and infusion of crystalloid should be started to support the patient’s blood pressure. Blood products may need to be administered to prevent cardiovascular collapse in the setting of maternal hemorrhage and shock or for correction of coagulopathy. Atropine may need to be administered for bradycardia due to increased vagal tone or impending cardiac arrest. Labs should be sent to monitor the hemoglobin and hematocrit for blood loss and check coagulation studies.4,8,12

  • Do not attempt to remove the placenta. If the uterus inverts before placental separation, detachment or removal of the placenta should not be undertaken as this may lead to worsening hemorrhage. Case reports describe severe hemorrhage occurring when the placenta is removed prior to manual replacement of the uterus.6,7 The presence of the placenta should not interfere with the clinician’s ability to restore the uterus to its normal position. Once the uterus is manually replaced, the clinician should await spontaneous separation of the placenta or manual extraction can be performed if indicated in the operating room.3,4,5,6

  • Immediately attempt to manually replace the inverted uterus to its normal position. This should be performed as rapidly as possible prior to formation of a cervical constriction ring. Manual replacement is achieved using the Johnson maneuver (Figure 28.3). Place a gloved hand in the vagina and push the uterine fundus along the long axis of the vagina toward the umbilicus, using the palm of the hand (holding the uterine fundus in the palm like a tennis ball) or using a closed fist. Caution should be taken not to perforate the uterus with the fingers by applying upward pressure circumferentially.1,4 If a constriction ring is palpable, pressure should be applied to the part of the fundus closest to the ring. This eases the fundus through the cervical opening from the lower uterine segment to the fundus, allowing for the narrowest diameter to pass through first.

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Dec 30, 2020 | Posted by in EMERGENCY MEDICINE | Comments Off on Uterine Inversion and Uterine Rupture

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